Hyperammonemia.

Naeem Aslam.
Fellow-2010
Univ. of Louisville. KY
 Contents of discussion.
„ Interesting Case.
„ Causes of high ammonia (cirrhosis is not only
cause)
„ Metabolism of ammonia.
„ Discussion about the case.
 Case
„ 39 yrs old AAF with h/o Gastric bypass (type
1) surgery in 2008 admitted for reversal of
bypass surgery.
„ Multiple admissions in the past for excessive
weight loss, weakness and peripheral
neuropathies secondary to weight loss.
„ Weighed around > 400 pounds in 03/08
„ Weighed 225 pounds in 04/09
„ Patient was diagnosed with multiple vitamin
deficiencies including B12, copper, iron and
thiamine and being supplemented.
„ Other issues
Anasarca.
Anemia of chronic disease.
Weakness- uses cane to walk.

PMH
Obesity s/p gastric bypass
„ Previous admission. Had elevated LFts and
found to have elevated ammonia level. Started
on Lactulose and carnitor. S/p Liver biopsy
„ Liver biopsy 04/09
Acute and chronic cholestasis and panlobular
macrovesicular steatosis. Mod. Portal
inflammation with lymphocytes and
histiocytes.
„ PSH
Gastric bypass surgery.
C-sections.

Social history- No smoking, no alcohol and no

drugs.
„ Medications.

Vitamin B1 250 mg once a day.

Vitamin B12
Calcium citrate plus D
Iron
MVI
ASA
Copper 2 mg PO once a day.
Carnitor 330 mg PO BID
Prilosec.
Lortabl
 Exam.
„ P. 100 BP 131/87 RR 20 sats 98%
Wasting-temporal. Prominent bones around clavicular
and spine area.
Alert orientedX 3
CVS s1 s2
Chest clear
Abdomen, distended, fluid thrill +
Edema 2+ b/l
CNS. Alert oriented X3 4/5 all limbs.
„ WBC 11.75
„ HB 11.5 MCV 86
„ Plt 346
„ N 75%
„ Total Bili 3.6 Direct 1.4
„ AST/ALT 62/62 Albumin 1.9
„ Alk. Phosph.
„ PT 17.9
„ INR. 1.9
„ PTT 32.7
 Hospital course
„ Admitted to get reversal of gastric bypass.
„ Started on TPN to build up.

TPN - 1225 Cal

60 GM AA
Dextrose. 635 Kcal
Lipid 350 Kcal
80% patient estimated Kcal.
Ensure supplements BID.
„ On 4th day of hospitalization patient got
confused and GI consulted for high Ammonia
level.
„ Patient got more worse and unresponsive with
Ammonia of 300 and transferred to ICU.
 Labs at that time.
„ Na 138 ABG 7.5/44/64/34/94%
„ K 4.4 PT/INR 16.5/1.7
„ CO2 31
„ BUN/CRT 12/0.6
„ Glucose 89
„ Total Bil. 3.8
„ AST/ALT 34/30
„ Alk Phosp 155
„ Ammonia 300
„ WBC 10.92
„ HB 10.6
„ PLT 210
„ N 79
 MRI Head.
„ No evidence of acute infarct.
„ No abnormal intensity or enhancement present
within the brain parenchyma.
„ No significant abnormal T1 signal seen within
basal ganglia.

„ EEG. Metabolic encephalopathy.

„ Folate. 8.0 (3-16)
„ B12 > 2100
„ Ceruloplasmin 14 (17-54)
„ Copper 78 (80-155)
„ Selenium 30 (23-190)
„ Zinc 31 52 (60-120)
„ Thiamine
„ Carnitine
 ?
„ History. Review of
history. Admitted
before- Got TPN and
ammonia went up.
„ Biopsy. Abnormal but
not cirrhotic.
„ ?
„ UREA CYCLE DEFECT ?
„ Serum Aminoacid panel and urine aminoacids
sent.
„ TPN stopped.
„ Started on buphenyl. Ammonia started
coming down. Patient got more responsive on
second day.
„ Genetic counseler consulted.
Æ Tube Feed diet of 60 gms of protein per day.
50% of protein. Natural protein
(ensure/boost)
50% provided through specialized formula
Cyclinex-2 (essential amino acids)
Æ Buphenyl
Æ Citrulline.
Protein (L-amino acids),
carbohydrates (corn syrup
solids), fat (high oleic
safflower, coconut, soy
oils), L-carnitine, taurine,
iron (ferrous sulfate),
vitamins, minerals; contains
phenylalanine; nonessential
amino-acid free.
 Corn Syrup Solids, High Oleic Safflower Oil,
„

Coconut Oil, Sodium Citrate, Soy Oil, L- „ Essential AA

Leucine, L-Lysine Acetate, L-Valine, Calcium
Phosphate, L-Isoleucine, Magnesium Phosphate,
Potassium Chloride, L-Tyrosine, L-Threonine,
phenylalanine, valine,
L-Phenylalanine, Silicon Dioxide, DATEM*,
Potassium Citrate, Potassium Phosphate, L-
threonine, tryptophan,
Cystine Dihydrochloride, L-Histidine, L-
Methionine, L-Tryptophan, L-Carnitine,
isoleucine, methionine,
Calcium Carbonate, Ascorbic Acid, Taurine,
Choline Chloride, m-Inositol, Ferrous Sulfate,
leucine, and lysine
Zinc Sulfate, Niacinamide, dl-Alpha-Tocopheryl
Acetate, Calcium Pantothenate, Ascorbyl
Palmitate, Mixed Tocopherols, Cupric Sulfate,
Manganese Sulfate, Thiamine Chloride
Hydrochloride, Vitamin A Palmitate, Riboflavin,
Pyridoxine Hydrochloride, Folic Acid,
Potassium Iodide, Chromium Chloride, Beta-
Carotene, Biotin, Sodium Selenate,
Phylloquinone, Sodium Molybdate, Vitamin D3,
and Cyanocobalamin.
 SERUM AMINOACID.
„ ALANINE. ISOLEUCINE.
„ ARGININE. LEUCINE.
„ ASPARTIC ACID. LYSINE.
„ CITRULLINE. METHIONINE.
„ CYSTINE. ORNITHINE.
„ GLUTAMIC ACID PROLINE.
„ GLUTAMINE SERINE.
„ GLYCINE. TAURINE.
„ HISTIDINE
„ HOMOCYSTINE.
„ HYDROXYPROLINE.
 24 URINE
„ OROTIC ACID SUBERIC ACID
„ LACTIC SEBACIC ACID.
„ PYRUVIC PHENYLACETIC ACID
„ SUCCINIC SUCCINLYACETONE
„ FUMARIC
„ KETOGLUTARIC
„ METHYLMALONIC
„ HYDROXYBUTYRIC
„ ACETOACETIC
„ KETOACIDS.
„ ADIPIC ACID
„ GLYCINE Æ 724 (140-490)
„ GLUTAMINE Æ 3210 (410-700)
„ CITRULLINE Æ 15, 11(10-60)
„ ARGININE Æ 59 (40-160)
„ ORNITHINE Æ 48 (20-135)
„ ISOLEUCINE - LOW
„ LEUCINE - LOW
„ LYSINE - HIGH
„ SERINE - HIGH.
„ GLYCINE Æ
724 (140-490)
„ GLUTAMINE Æ
3210 (410-700)
„ CITRULLINE Æ
15, 11(10-60)
„ ARGININE Æ
59 (40-160)
„ ORNITHINE Æ
48 (20-135)
 URINE.
„ OROTIC ACID. 8.0 (.8-2.7)
 Genetic testing.
„ Blood sample.
„ OTC deficiency-Gene deletion/duplication.
Sequence analysis did not identify mutation.

OTC Full Gene squencing. One homozygous

(2 copies) variant c 137 A-G in the OTC gene
.
 Repeat AA panel in 6 weeks
„ Citrulline. 107 H (10-60)
„ Arginine 105 (40-105)
„ Ornithine 105 (20-135)
„ Glutamine 368 L (410-700)
„ Glycine 332 (140-490)
„ Liver biopsy. 09/2009
Macrovesicular steatosis portal and pericellular
fibrosis and progressive cholestasis.

Comment by pathologist. Fatty change and

pericellular fibrosis has been reported as
possible feature of OTC deficiency.
 Ascites fluid
„ Fluid protein. 647 mg/dl
„ Fluid Albumin <1.5
„ WBC 6
 USG
„ Echogenic liver with slight nodular contours.
This may represent fatty infilteration but
cirrhosis cannot be ruled out.
„ Large volume ascites.
„ Gall bladder with sludge.
 Doppler USG.
„ Non occlusive thrombus-portal vein.
„ Ascites.
Ammonia Metabolism.
 Elevated Ammonia.
„ Production.
„ Metabolism.
„ Excretion .
Which organ is involved in ammonia
metabolism.? T/F
„ Gut
„ Kidney.
„ Muscle.
„ Liver.
„ Brain.
„ None of the above.
„ All of the above.
Which organ is involved in ammonia
metabolism.? T/F
„ Gut
„ Kidney.
„ Muscle.
„ Liver.
„ Brain.
„ None of the above.
„ All of the above. True.
► Gut. Byproduct of protein digestion
and bacterial metabolism.

► Kidneys. Essential for renal handling of

acid. Ammonium is synthesized from
glutamine (proximal tubule) either released
into systemic circulation or excreted.
(Hyperammonemia in the ICU. Chest. 2007:132:1368-1378)
►Skeletal muscle. Seizures or intense exercise
increased ammonia production.
 Ammonia degradation.
„ Liver is primarily responsible for ammonia
degradation.
„ Ammonia is metabolized by urea cycle.
„ In case liver does not metabolize or more
ammonia which liver can handle elimination is
dependent on the kidneys, muscle and brain.
„ Kidneys. Increase urinary excretion of
ammonia.
„ Muscle and brain. Metabolize ammonia to
glutamine.
 Brain and glutamine.
„ Acute rise in ammonia.
Astrocytes rapidly metabolize ammonia to
glutamineÆ increased intracellular osmolarityÆ
cerebral edema + inflammatory cytokine releaseÆ
Apoptosis
Excessive activation of NMDA (glutamate)
receptorsÆ neuronal degeneration and death.
 Mechanizm of CNS injury.

„ Intracerebral accumulation of glutamine is the major

cause of encephalopathy.

„ High level of ammonia result in conversion of

glutamate to glutamine by glutamine synthetase
which occurs in astrocytes.

„ Increased intracellular osmolality results in astrocytic

swelling, brain edema and cerebral hypoperfusion.
 Role of MRI in Acute Hyperammonemic
Encephalopathy.
„ Four groups.
a. Diffuse cerebral Edema followed by
diffuse cerebral atrophy.
b. Extensive infarct like abnormality
presenting as acute hemiplegia.
c. Ischemic lesions in cerebral vascular
territory.
d. Reversible symmetric cortical involvement of cingulate
gyri, temporal lobes and insular cortex.

(Takanashi J. Brain MR imaging in neonatal hyperammonemic

encephalopathy resulting from proximal urea cycle disorder. Am J
Neuroradiology)
 . A, Image done on admission to the
community hospital. B, Image done 24 hours later demonstrates
bilateral hemispheric edema with effacement of cerebrospinal fluid
spaces
Hyperammonemia in OTC deficient patient.
 Venous or Arterial Ammonia.?
Which is better to check ?
 Venous or Arterial Ammonia.?
► Liver is working.
Venous and arterial ammonia do not correlate. As
liver metabolize venous ammonia.

► Fulminant hepatic failure.

Venous ammonia correlate with Arterial ammonia.
Arterial ammonia correlate with brain glutamine
level which correlate with development of ICH
(intracranial Hypertension).
 Consult of increased ammonia.
„ Increased ammonia production.
„ Decrease Ammonia elimination.
 Increased ammonia production.
„ High protein load and increased catabolism.
„ Seizures.
„ Trauma or burns.
„ Steroid administration.
„ Starvation.
„ GI hemorrhage.
„ TPN
„ Urease producing bacteria (proteus, klebsiella) infection.
„ Severe exercise.
„ Chemotherapy.
„ Cancers. (multiple Myeloma)
 Decreased Ammonia Elimination.
„ Liver Failure.
„ TIPS.

„ Drugs.

„ Inborn errors of metabolism.

Urea cycle disorders.

Organic acidurias.
 Drugs associated with
Hyperammonemia
A. Drugs causing liver failure.
B. Drugs associated with UCDs.
Glycine.
Salicylates.
Valproate.
Carbamezipine.
Sulfadiazine.
Pyrimethamine.
 Work up for high Ammonia
„ History is very important.
„ Rule out liver disease. Blood/Imaging
„ Two conditions can co-exist.
„ Medications.
„ Consider inborn errors of metabolism.
UREA CYCLE.
 UREA cycle disorders.
„ Carbamyl phosphate synthetase deficiency.
„ Ornithine transcarbamylase deficiency.
„ Arginosuccinate synthetase deficiency.
„ Arginosuccinate lyase deficiency.
„ N-acetyl glutamate synthetase deficiency.
„ Arginase deficiency.
„ Epidemiology.
1 in 8200 live births

Pathophysiology.
Urea cycle converts nitrogen from peripheral
(muscle) and enteral source (protein ingestion)
into urea that is water soluble and excreted.
„ Two moles of nitrogen one from ammonia and
one from aspartate are converted to urea in
each cycle.
„ Ammonia nitrogen derives from circulating
aminoacids, mostly glutamine and alanine.
„ Aspartate is a substrate for arginosuccinic acid
synthesis.
„ NAGs, OTC, CPS are located in mitochondria,
primary mitochondrial disease may affect urea
cycle activity.
 Genetics.
„ All UCDs are autosomal recessive except
„ OTC deficiency- X linked.

All female offsprings of a male OTC-deficient

parent will carry an OTC mutation and 50% of
all offspring from a female OTC deficient will
carry the mutation.
„ 10% of female carriers of OTC become
symptomatic.
„ Clinical severity in affected females depends
on the pattern of X-inactivation in the liver
(lyonization) and ranges from asymptomatic to
severely symptomatic.
„ Hemizygous males usually are more severely
affected than are the heterozygous females.
 Clinical presentation.
„ Mostly seen in newborns. Partial enzyme deficiency
may become symptomatic later in life.
„ Typical symptoms. Once feeding is started (human or
infant formula)
Somnolence and poor feeding.
Vomiting.
Lethargy.
Coma.
ÆHyperventillation (cerebral edema) then
hypoventillationÆabnormal posturing and resp.
arrest.
ÆAtypical presentation. Partial enzyme deficiencies.
Chronic vomiting, developmental delay, seizure
disorder, headache, lethargy.
Æ Protein intake/catabolic stateÆmake them worse.

Æ Prefer vegetarian diet.

 When do you suspect urea cycle
disorder.
„ Elevated ammonia with normal LFTs.
„ Labs to be ordered.

Serum ammonia.
ABGs
Urine organic acids. Normal
Serum AA
Urinary orotic acid.
 Genetic causes of Hyperammonemia.

„ Organic acidemias result from inhibition of

one of the urea cycle enzymes. (metabolic
acidosis/and or ketotic hypoglycemia)
„ Fatty oxidation defects. Non- ketotic
hypoglycemia.
„ Disorders of pyruvate metabolism. Lactic
acidemia usually seen.
Clinical approach to a newborn infant with symptomatic
hyperammonemia.
(Kliegman)
 Rare causes

„ HHH syndrome. (Hyperornithinemia,

hyperammonemia, homocitrullinemia.) Impaired
transport of ornithine across inner mitochondrial
membrane. Presents with Lethargy, hypotonia and
seizures.

„ THAN (transient hyperammonemia of the newborn) –

Low birth weight , respiratory distress.
 Lab evaluation.
„ Elevated ammonia.
( arterial or venous.)

Chilled tubes with ammonia-free sodium heparin

(green top) or EDTA (purple top), placed on ice.
 Ammonia Levels.
Ammonia level higher in newborns.
Healthy term infant- 45 mean (upto 90 micromol/L)
At 32 week preterm 71 micromol/L
Children >1 month Less than 50 micromol/l
Adults less than 30 micromol/l
„ Quantitative plasma aminoacids.
„ Citrulline level. Absent or low in CPSI, OTC
or NAGS.
„ Arginine is low
„ Glutamine is increased.
„ Urine orotic acid increased in OTC
normal 1-11 micromol/mol creatinine) ,Low in
CPS
 Increased Glycine and
Glutamine.

Low Citrulline Increased Citrulline.

Check orotic acid. Check Arginine.

Increased Orotic acid. Normal Orotic acid. Normal Arginine. Increased Arginine.
OTC deficiency. CPS deficiency. Urine Arginosucinate Arginine deficiency.

No Arginosuccinate.
Citrullinemia

Arginosuccinate in urine
Acetylsalicylic acid deficiency
Enzyme Plasma Citrulline Arginosucc Orotic acid Arginine/or
deficiency ammonia inate (urine Urine nithine
or serum) serum
Carbamyl High Low Low Low Low
phosphate
synthetase
OTC High Low Low High Low

Arginosucc High High Low Normal or Low

inate high
synthetase
Arginosucc High High High Normal or Low
inase high
Arginase High High High Normal or High
high
 Enzyme analysis
„ Liver biopsy: CPSi, OTC and NAGs
deficiency.
„ Fibroblasts from skin biopsy. ASS and ASL
deficiency.
„ Red blood cells: Arginase deficiency.

(Levels may be normal)

 Specialized testing (research)
Allopurinol test.
Measurement of urinary orotic acid after
administration of allopurinol. Mild cases may
have minimal elevation.
Increased excretion may occur in
mitochondrial disease limiting specificity.
 DNA mutation analysis.

More than 150 mutations mostly single base

substitutions.
„ OTC is most common DNA testing should be
considered if plasma AA is not diagnostic.
„ False negative results (microdeletions).
„ Failure to detect a pathogenic mutation does
not exclude the diagnosis.
 Prenatal testing.

1. DNA analysis. (if mutation is known)

OTC and CPSI deficiency.

2. Biochemical testing. ASS and ASL enzyme

activity can be measured in amniocytes and
chorionic villus cells.
 Management of Urea cycle disorders

► Start treatment as soon as UCD is suspected.

► Rehydration with good urine output.
► Remove nitrogen
Medicines and hemodialysis
Decrease or stop protein intake.
Minimize catabolism.
Stimulate anabolism and uptake of nitrogen
precursors by muscle.
► Control infection.
► Avoid.
Steroids. Increase catabolism.
Valproic acid. Decrease urea cycle, and
increase ammonia level.
„ Hemodialysis.
For severe hyperammonemia.
Continous Arteriovenous or Venovenous
hemodialysis (CAVHD or CVVHD) with flow rates
> 40-60 ml/min
 Pharmacologic therapy

„ Removal of Glutamine and Glycine to

reduce total nitrogen pool.
- Phenylacetate combine with glutamine to
form Phenylacetylglutamine.
- Benzoate combines with glycine to form
hippurate.
- Both phenylacetylglutamine and hippurate are water
soluble and excreted in urine.
 Ammonul (sodium phenylacetate-sodium
benzoate)
„ Approved in 2005 for parenteral delivery.

<20 Kg loading dose of 500 mg/kg in a

volume of 25-35 ml/kg of 10% dextrose
infused over 90 minutes.

>20 Kg, dosing is based on surface area.

Loading dose is 11 g/m2
„ Maintenance infusion is continued until oral
medications can be tolerated.
(500 mg/kg per 24 hrs < 20 Kg.
11 g/m2 per 24 hrs for > 20 Kg)
„ Adverse Effects of Ammonul.
Metabolic. Hypokalemia, Hyperchloremia,
acidosis)
Neurologic (seizures)
Resp. distress/failure.
Buphenyl (Sodium phenylbutyrate)
„ The usual daily dose of BUPHENYL Tablets
and Powder is:
450 – 600 mg/kg/day for patients <20 kg,
or
>9.9 – 13.0 g/m2/day in larger patients.
 Adverse Events of Buphenyl

„ Amenorrhea/menstrual dysfunction.
„ Decreased appetite occurred in 4% of all
patients.
„ Body odor (probably caused by the metabolite
phenylacetate) and bad taste or taste aversion
were each reported in 3% of patients.
„ Metabolic: acidosis (14%), alkalosis and hyperchloremia (each
7%), hypophosphatemia (6%), hyperuricemia and
hyperphosphatemia (each 2%), and hypernatremia and
hypokalemia (each 1%)
„ Nutritional: hypoalbuminemia (11%) and decreased total
protein (3%)
„ Hepatic: increased alkaline phosphatase (6%), increased liver
transaminases (4%), and hyperbilirubinemia (1%)
„ Hematologic: anemia (9%), leukopenia and leukocytosis (each
4%), thrombocytopenia (3%), and thrombocytosis (1%)
 Arginine

„ Decreased formation of Arginine making it essential

aminoacid.

„ Arginine deficiency leads to catabolic state resulting

in more protein breakdown and mobilization of
nitrogen.

„ Decrease formation of ornithine, citrulline and

Arginosuccinic aced. Providing arginine generate
these water-soluble compounds that can be excreted
and results in removal of NH3
„ Dose
IV Arginine hydrochloride.
Loading dose
<20 Kg loading dose 600 mg/kg dissolved in 25-35
ml/kg of 10% dextrose infused over 90 minutes.
>20 kg loading dose is 12 g/m2
„ Maintenance dose.
200 mg/kg per 24 hrs. <20 kg
4 g/m2 per 24 hrs >20 Kg

For ASS and ASL deficiency higher maintenance

dose of 600 mg/kg used to increase generation of
citrulline and Arginosuccinic acid.
 Citrulline

„ OTC and CPS deficiency.

Oral dose of citrulline
150-250 mg/kg per 24 hrs <20 kg
3-4 g/m2 per 24 hrs > 20 kg.
 What to monitor during therapy

Æ Electrolytes and routine labs. Potassium and sodium.

Æ Ammonia every hour during dialysis and once stable below
200 micrmol/L for 24 hrs measurement can be reduced to
every 4 hrs.
Æ Serum Aminoacids are measured (daily) to assess efficacy
of glutamine removal and to determine replacement of
Arginine or citrulline
 Protein Restriction.

„ Infants.. 2-2.5 gm/kg per day

„ Adults. 0.6-0.8 gm/kg
Children require less than recommended daily intake
of protein for normal growth. Patient with partial
deficiency of urea cycle may tolerate greater protein
intake.
„ In acute hyperammonemia oral feeding is
discontinued
„ Calories are provided by IV administration of
lipids and glucose and protein intake is
stopped.
„ Protein should not be stopped more than 24-48
hrs after treatment to avoid protein catabolism
„ Enteral feeding is initiated as soon as possible
„ Protein free formula such as Mead johnson or

Ross formula Prophree in conjunction with

amino acid mixtures and cow milk based
formulas.
(less Nitrogen in aminoacid mixtures)

Pro-phree (abbott). Protein free, L carnitine, linolenic acid,

vitamins
„ Measure serum levels of essential aminoacids
(branched chain AA, phenylalanine, lysine). Samples
are obtained 3-4 after feeding and repeated every 2-3
days.

Chronic management. Weight and growth

total protein, albumin and prealbumin.
 Nutritional deficiencies following Bariatric
Surgery: What have we learned?
„ Protein Deficiency.
„ Iron deficiency.
„ Vitamin B12 and Folate deficiency.
„ Calcium and Vitamin D deficiency.
„ Thiamine (vit. B1) deficiency.
„ Fat soluble Vit. Def. Vit A, E, K
„ Magnesium.
„ Zinc
„ Selenium.

(Obesity Surgery, 15. 2005)

 Routine laboratory testing after malabsorptive
bariatric surgery

3 months postoperatively. Complete blood count;

glucose; glycosylated hemoglobin[a]; lipids; chemistry group

At 6-month intervals during first 3 years & then once

yearly
Chemistry ; complete blood count; lipids; ferritin; zinc;
copper; magnesium; vitamin A; total 25-hydroxy vitamin D;
folate; whole blood thiamine; vitamin B12; 24-hour urinary
calcium
(Postoperative Metabolic and Nutritional Complications of Bariatric Surgery
Gastroenterology Clinics - Volume 39, Issue 1 (March 2010)
 General supplementation recommendations.
(RYGB-Roux Y gastric Bypass, VSG vertical sleeve gastroplasty, AGB- Adjustable Band,
BPD- biliopancreatic diversion, BPD-DS –biliopancreatic diversion with duodenal switch)

Multivitamin containing AGB/VSG Once daily

folic acid RY GB 1-2 daily
BPD-DS 2 daily.
Calcium citrate with AGB 1200-1500 mg/day
Vitamin D3 RYGB and BPD-DS 1800 mg/day
Vitamin D3 RYGB 1000 IU/day
BPD-DS 2000 IU/day
Vitamin B12 RY GB Orally or 1000 ug/month
IM
BPD-DS Monitor and start if needed
Elemental Iron RYGB and BDP-DS 65 mg elemental iron in
mensturating females.
Vitamin B1 All procedures Once daily in first 6 months
Vit A and Vit K BPD-DS 10,000 IU vitamin A and
300 ug vitamin K
 Laboratory testing for nutritional disorders
after bariatric surgery

„ Anemia Ferritin; vitamin B12; folate & then consider vitamin

A; vitamin E; zinc; copper
„ Neurologic disorders. Vitamin B12; whole blood thiamine &
then consider vitamin E; copper; plasma niacin
„ Visual disorders. Vitamin A; vitamin E; whole blood thiamine
„ Skin disorders. Vitamin A; zinc; plasma niacin
„ Edema Selenium; whole blood thiamine; plasma niacin

(Postoperative Metabolic and Nutritional Complications of Bariatric Surgery

Gastroenterology Clinics - Volume 39, Issue 1 (March 2010)
„

„ Thank you.